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Unformatted text preview: "W” "the impairment'i’s’p‘e’rmanent. " The Structure and Mechanisms of Memory Alan ]. Perkin Memory, of all the powers of the mind, is the most delicate and the most frail. Ben Johnson The study of human memory disorder has a long history, making it, perhaps, the oldest topic within neuropsychology. As with most areas of psychology, longevity is no guarantee of theo- retical development and, in many ways, amnesia remains as much a challenge now as it did 50 years ago. In this chapter I will discuss the contribution that research into human amnesia has made to our understanding of normal memory and will conclude by considering the direction of future research into human memory disorder. WHAT IS AMNESIA? The term amnesia is so general as to be largely meaningless except as an indication that someone has a faulty memory. As we shall see, memory can go wrong in many different ways and this has major implications at both theoretical and clinical levels. The first distinction we must make is between psychogenic disorders (also known as functional disorders) and those whose origin is organic. Psychogenic disorders are losses of memory which arise following psychological trauma. They can be classified into a number of subtypes. Most common is dissociative or hysterical amnesia in which there is a partial loss of memory for events surrounding a traumatic event. Other types include post-traumatic stress disorder (PTSD), fugue, and multiple personality disorder. Their existence has proved valuable as a device in fiction but their frequency of occurence in 'this context betrays a scant knowledge of how memory impairment can arise as a consequence of psychological trauma. ,, ., Organic disordersrarebyfar,the“most impo'rtantrfrom, $119,139,131“, of viewwqf CygnitiVe neurop- sychology. They exist in two essential subtypes: (a) transient, where memory function is im-fl paired for a limited period, following which normal functioning returns; and (b) chronic, where The most well-known transient organic disorder is transient global amnesia (TGA) in which the person experiences a severe loss of memory which can range from a few hours to several days. There is a degree of systematicity in the pattern of recovery (Kapur, Millar, Abbott, & Carter, 1998) and usually only events during the TGA period itself are permanently lost 7 400 Memory . (Hodges, 1998 . TGA has been associated with epilepsy and electroconvulsive therapy (ECT). Because of its duration and systematic availability, post-ECT amnesia is the only transient state which has received extensive investigation at a cognitive level, but there is continuing controversy about the possible long—term effects of ECT (Parkin, 1997c). The cognitive neuropsychology of memory has focused mostly on patients with chronic disorders of memory. These include the dementias, in which there is a gradual loss of memory, focal retrograde amnesia, where the primary deficit is a loss of memory for the past, and the amnesic syndrome, which is dominated by a severe and permanent anterograde amnesia.1 Most of the research discussed in this chapter involves the amnesic syndrome and ed it would be useful to review the syndrome’s characteristic features at this point (in Parkin, 1997c. wiww~app:~87-883.7Theywareaasrfollows:7 , m , 7 7 l. Unimpaired short-term storage as measured by tasks such as digit span. 2. A severe and permanent anterograde amnesia, with exceptionally poor performance on tests of recall such WMS—R hard-paired associate learning. WMS-R logical memory and visual reproduction scores are very low. Recognition is also poor, with chance perfor- mance often observed on- tests such as RMT. 3. Semantic memory, and other intellectual functions, as measured by tests such as WAIS- R, are generally intact. Thus, to be classified as amnesic a patient would have an average IQ but scores on the WMS-R indices (especially the delayed memory index) would be well below normal levels. _ 4. Skill learning, conditioning, perceptual learning, and priming are relatively intact. 5. Retrograde amnesia will inevitably be present but its extent can be extremely variable with some patients having extensive deficits and others lacking memory only for very recent parts of the premorbid period. THE NEURAL BASES OF MEMORY AND AMNESIA Figure 16.1 illustrates the various brain structures which, when damaged, can give rise to the amnesic syndrome. These structures occur in two distinct areas of the brain, the midline diencephalon and the medial temporal lobes. Much of what we know about the amnesic syndrome has stemmed from investigations of patients with Korsakoff’s Syndrome. These patients have suffered damage to a variety of diencephalic structures, most notably the dorso—medial thalamic nucleus, the mamillary bodies, the mamillo-thalamic tract, and certain areas adjacent to the third ventricle. However, there is also a degree of cortical involvement, especially in the frontal cortex, and more recently it has been pointed out that Korsakoff patients may have additional damage in the medial temporal lobe. Although Korsakoff’s Syndrome is the primary cause of amnesia arising through damage to the diencephalon, there are other causes. The thalamic region is prone to vascular disorders which can give rise to amnesia (Parkin, Rees, Hunkin, & Rose, 1994; see Figure 16.2). Dien— cephalic amnesia can also arise from the presence of tumours (Parkin & Hunkin, 1993b). The floor of the third ventricle is adjacent to diencephalic structures and tumors here can exert local pressure on those structures, causing memory loss. Tumors can also damage the mamillary bodies, as can paranasal penetrating head injuries (Dusoir, Kapur, Byrnes, McKinstry, & Hoare, ,1990). A case of paranasalpenetrating head injury involving more extensive damage is NA. , When he was first scanned it was claimed that he had a lesion restricted to the dorso—medial nucleus of the thalamus. More detailed neuroimaging has since shown much more extensive damage, 1ncl'i1ding complete d'és’tructmn’of thé’inamillary’bodies?Signiffihntlifihowefir,’ there is no damage to the hippocampal formation (Perkin, 2000b). lRetrograde amnesia refers to an inability to remember things known prior to the precipitating trauma or illness. Anterograde amnesia refers to difficulty in acquiring new information following the trauma or illness. The Structure and Mechanisms of Memory 401 Cingulate gyrus VieriFrontalelobe? Thalamus‘ Septum Hippocampus* Olfactory bulb Reticular H othalamus formation ‘yp Mammillary Amygdala body* Spinal cord Figure 16.1: Diagram of the limbic system and related structures. Areas indi— cated with an asterisk are known to be associated with memory function. Involvement of the temporal lobes in memory was only firmly established in the 1950s, although it had long been suspected from isolated clinical reports. The evidence came from temporal lobectomy in which areas of the temporal lobe responsible for epileptic seizures were selectively removed. The most famous of these patients is HM, whose dense amnesia I have discussed in detail elsewhere (Parkin, 1996b). Notes talten during his operation and others led to the View that the critical structure involved in amnesia was the hippocampus. However, conclusions about HM’s underlying pathology must now be qualified by the discovery that he also has significant atrophy of the mamillary bodies, at least in the present day (Corltin, Amaral, Gonzalez, Johnson, & Hyman, 1997). A patient with selective damage to the CA1 field of the hippocampus resulting from a small ischaemic lesion has been described by Zola—Morgan, Squire, and Amaral (1986). RB exhibits anterograde amnesia with little evidence of retrograde amnesia. In a follow—up study it has been argued that lesions restricted to CA1 essentially produce anterograde amnesia alone, . whereas more extensive damage, although still restricted to the hippocampal formation, gives "rise'to 'anterograde amnesia and an extensive retrogradeamnesia '(Re’mpeLClower, Zola, Squire, " ' & Amaral, 1996). amnesia following hippocampal pathology have largely relied on survivors of herpes simplex encephalitis. This is a viral infection of the brain that rapidly causes extensive brain damage centred on the temporal lobes, MRI scans of patients who survive this illness invariably show hippocampal lesions but the damage is always more extensive than this, extending most com- monly into the temporal cortex and the prefrontal cortex (especially orbito-frontal). There is iSrelective ischaremici lesions of the 11112130951de formation are, rare and attempts to examine ,, ./ .. ‘.,-.r...._l._.~_...-s.m “W“-.. ... . :- l l: g i _: 1 1 11 l 402 Memory Figure 16 2: MRI scan of patient IR Note the dark region in the centre A small lesion in the region of the dorsomedial nucleus of the thalamus little indication that herpes simplex encephalitis leads to any significant damage to the dien— cephalic structures identified with amnesia (Parkin & Leng, 1993). The question of whether there are two forms of amnesia arising from damage to two differ- ent areas of the brain (the midline diencephalon and the medial temporal lobes) is not easily answered because the data are not as “clean” as one would like. Firstly, as we have seen, the ' major sources of “diencephalic’ and “temporal lobe” amnesia stem from aetiologies which produce large lesions extending beyond those structures assumed to be crucial to the memory impairment. Secondly, we may be restricted by the accuracy of the neuropathological informa- tion available as, for example in the case of HM who has now been shown to have additional diencephalic damage. There are, therefore, relatively few cases of the amnesic syndrome' in which we can be confident there is no overlapping lesion. Another important fact to bear in mind when considering the various lesion sites which to the anterior thalamus both directly, via the fornix, and indirectly, via the mamfllary bodies i and mamillothalamic tract. There are further projections from the anterior thalamic'nucleus to ' 43% r. p ”5‘ ‘ . a.» c. 72W “I" ‘ egg ES" , ; I? w . . x L l g... . ‘9 sag ‘5 WE ”3% CELT: ”v (2 as re . r as: ; g _ . . , a. . s. ,, .. «M an .. m The Structure and Mechanisms of Memory 403 cingulate and frontal cortex as well as projections back to the hippocampus and adjacent cortical areas via the cingulum. If memory relied on a “circuit” then damage anywhere along that circuit could disrupt memory functioning. THE STRUCTURE OF MEMORY The Dichotomy between Short and Long Term Storage (STS and LTS) William James’ seminal distinction between primary and secondary memory (James 1890) had, by the end of the 19605, transformed into the dichotomy between short— and long-term store (STS and LTS) (Atkinson & Shiffrin, 1968). Various lines of evidence from normal subjects were put forward in support of this dichotomy. Further evidence came from patients who had suffered lesions to the hippocampus as a result of temporal lobectomy, the most well- known of these patients being HM. Atkinson & Shiffrin considered this line of evidence pro- vided “perhaps the single most convincing demonstration of a dichotomy in the memory system” (p. 97). Milner (1966) reported that patients with bilateral surgical lesions in the hippocampal region shows a severe and persstent disorder of memory. Although material known prior to the operation ' remained intact, patients were unable to acquire further information. Immediate registration of new information seemed to take place normally and material which could be rehearsed verbally was retained for many minutes without loss. However, material which could not be verbalized decayed in a matter of seconds, and interruption of rehearsal led to immediate loss. The pattern of impairment is the most consistent feature of all patients presenting the amnesic syndrome, regardless of etiology They invariably show normal range performance on tests of immediate apprehension such as digit span alongside marked impairments of longer— term retention (Parkin & Lang, 1998). Indeed, without the evidence from amnesia the STS/ LTS distinction would be rather shaky. Functional double dissociation of the serial position curve in unimpaired subjects, so long considered as incontrovertible evidence for the STS/LTS distinction, is now thought to reflect differences 1n strategic influences on memory. Otherwise, only a few drug studies provide support for the STS/LTS distinction (Perkin, 2000a). The Nature of LTS: Distinctions between Episodic, Semantic, and Procedural Memory By the early 1980s the pattern of deficits in amnesic patients was also forming an important foundation for theories concerning the organization of LTS. Anecdotal observations had, across many years, documented residual learning by amnesic patients in a variety of situations. In a detailed summary of these findings (Parkin, 1982) it was noted that amnesic patients retained skills acquired in the premorbid period and, at a more limited level, acquired new skills in the postmorbid period. Therewas also evidence of perceptual learning, classical and operant c011- »._. ditioning, alteration of verbal preferences, and even concept formation Despite their wide .1 , variation, one factor links all these instances of residual learning: in no case did patients have any significant recollection of the events that gave rise to this learning. Thus descriptions of ._ residual learning were consistently accompanied by comments such as. When shown the [closure] pictures again, one hour later, H.M.‘s performance improved by 48%, } although he did not remember having taken the test before.” (Milner, Corkin, & Teuber, 1968, p. l 230) Observations of this kind quickly became an essential component for theories proposing that LTS was best regarded as a tripartite structure comprising episodic, semantic, and procedural 404 Memory ’ ___________________—_.————-————-———- ll . . memory (Tulving, 1985). This proposal drew distinctions between memory which is consciously “ accessible and that which is not (episodic/ semantic versus procedural), and between memory , which involves recollecting a specific past event and that which does not (episodic versus semantic). The nature of LTS in amnesic patients had a direct bearing on both distinctions Little controversy surrounds the view that data from amnesics supports the distinction between episodic/ semantic memory on the one hand and procedural memory on the other. As well as the evidence documented in Parkin (1982) there has been a wealth of new evidence supporting preserved procedural memory in amnesic patients (Parkin & Leng, 1993). Nonethe- less it should be pointed out that this evidence does not support the existence of a “prOCedural memory system”; it supports the idea that there are a variety of learning systems within the cognitive system that operate outside the sphere of cognitive awareness/penetrability. Further- Imore, it can be speculated that these procedural abilities show the closest”affinity’with’thet"an'**v**"**~w~v~ learning capabilities of other animals. In contrast, the idea that amnesia supports the distinction between episodic and semantic memory is a matter of some considerable argument. At a clinical level it is quite easy to be convinced that amnesia results in a selective failure of episodic memory. Thus an amnesic patient will typically converse normally and show relatively unimpaired performance on tests of intelligence and language. In contrast, memory for ongoing events, such as a previously presented word list or the lunch time menu, will be severely disrupted. This relative imbalance in performance was held to support the relative sparing of semantic memory (the system underlying language and general knowledge) from episodic memory (the system needed for recollecting specific events; Tulving, 1985). Unfortunately this seemingly straightforward conclusion is marred by one major problem— the tests used in the original formulations of this argument were not equally sensitive. Put simply, the tasks used to test preserved semantic memory were easier than those used to test episodic memory. A key line of evidence for the claim that amnesic patients have normal semantic memory is their normal performance on intelligence tests like the WAIS—R. However, it has been pointed out that these tests deal primarily with information already acquired by early adult life. This creates a major problem because retrograde amnesia exhibits a temporal gradient—the earlier that information is acquired in life, the less vulnerable it is to the effects of a brain lesion (see later section). As a result, normal performance on WAIS-R is not a sensitive test of spared semantic memory (Squire, 1987). The point is illustrated by the case of PZ, a university professor who became amnesic shortly after writing his autobiography (Butters, 1984). As one would expect, his ability to recall episodes portrayed in his autobiography showed a marked temporal gradient, with only those from the 19205 intact. However, when his semantic memory for scientific terms was assessed he showed a similar retrograde amnesia and was only able to define those terms acquired earlier in his career. This parallel loss of event memory and general knowledge has also been demonstrated elsewhere. For example, Verfaellie, Reiss, and Roth (1995) have shown that Korsakoff patients are poor at defining words that came into use during the decades for which they have a dense amnesia for events. , Doubts about the episodic/ semantic distinction have led the majority of researchers to use the umbrella term declarative memory—referring to any memory that is consciously accessible. This solves some of the problems raised above for the episodic/ semantic distinction but there is the odd case which it does not easily handle. RFR became densely amneSic as a result of . ' herpes simplex encephalitis (Warrington ‘& McCarthy, 1988); He could retain little information ~ ~ , . ~ , , , I , on standard memory tests and could not even identify close friends and family. It was thus Finn," surprising {undiscover thatihe had nonetheless learned the meaning of new words and abbrevia- tions (e.g., AIDS) that had come into use during the period for which he was now amnesic. In addition he retained a remarkable ability to describe his friends in a general sense, even though he could not remember any event involving a particular person. There are now other The Structure and Mechanisms of Memory 405 i instances of remote memory breaking up in selective ways. For example, Kapur, Young, Bateman, i I and Kennedy (1989) described a dense amnesia for public events with intact personal event . memory, and the converse was described by O’Connor, Butters, Miliotis, Eslinger, and Cermak (1992). . , The episodic/ semantic debate has received new impetus from the study of children who have suffered brain lesions that disrupt memory. Vargha—Khadem et a1. (1997) described three pa- tients (aged 14—22 yrs) with brain injuries that occurred at birth, age 4, or age 9. MRI revealed bilateral hippocampal pathology in all three cases. Despite their pronounced amnesia for every- %* "WW ,1 ,,, rrmrr'i *VdayWeventsrall‘ threepatientsattendednormal’schoolsand’attained' ’l'evelS'oflanguage’compe?’*’ ,, m i ‘ tence, literacy, and factual knowledge within the low average to average range. On the basis of these findings it was suggested that the episodic and semantic components of memory are partly dissociable, with only the episodic component being fully reliant on the hippocampus. (See also Mishkin, Vargha—Khadem, & Gadian, 1998.) ‘ Ahern, Wood, and McBrien (1998) described a 9-year—old male whose amnesia resulted from congenital brain damage. Memory, attention, vocabulary, and reading sk...
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